The Distribution Kinetics of Topical<sup>14</sup>C‐Sulfur Mustard in Rabbit Ocular Tissues and the Effect of Acetylcysteine

Amir, Adina; Kadar, Tamar; Chapman, Shira; Turetz, J.; Levy, Aharon; Babin, Michael C.; Ricketts, Karen M.; Brozetti, J.; Logan, Thomas P.; Ross, Michelle

doi:10.1081/cus-120026300

Cited by 7 publications

(9 citation statements)

References 20 publications

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“…Various studies were performed on the rabbit eye to assess the treatment regime in SM-exposed eyes [Amir et al, 2000[Amir et al, , 2003Babin et al, 2004;Kadar et al, 2014] as mentioned above. Various studies were performed on the rabbit eye to assess the treatment regime in SM-exposed eyes [Amir et al, 2000[Amir et al, , 2003Babin et al, 2004;Kadar et al, 2014] as mentioned above.…”

Section: Management Of Acute Ocular Lesionsmentioning

confidence: 99%

Ocular Effects of Sulfur Mustard and Therapeutic Approaches

Panahi

Rajaee

Sahebkar

2017

J of Cellular Biochemistry

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Sulfur mustard (SM) is a strong blistering, highly reactive, lipophilic chemical war agent that causes injury in different organs including the skin, eyes, and respiratory tract. The Eyes are especially susceptible to the consequences of SM poisoning because of the aqueous and mucosal nature of conjunctiva and cornea. DNA alkylation and depletion of glutathione, are the most important mechanisms of SM action in the eye injuries. Acute clinical symptoms are including decrease in visual acuity, dryness, photophobia, blepharospasm, conjunctivitis, and complaints of foreign body sensation and soreness that gradually progress to severe ocular pain. Corneal abrasions, ulcerations, vesication, and perforations are common corneal consequences in SM injured victims. Appearance of chronic symptoms has been reported as chronic inflammation of the corneal and conjunctival vasculature, ischemia, lipid and cholesterol deposition, scarring in cornea, corneal thinning, opacification and perforation of the cornea, limbal stem cell deficiency (LSCD), and neovascularization. Different medical and surgical protocols have been documented in the management of SM-induced ocular injuries, including preservative-free artificial tears, topical steroids and antibiotic, mydriatic, antiglaucoma drops, therapeutic contact lenses, dark glasses and punctal plugs/cauterization, N-acetylcysteine, tarsorrhaphy, amniotic membrane transplantation, stem cell transplantation, and corneal transplantation. New drugs such as resolvin E1, topical form of essential fatty acids, thymosin β4, 43 amino-acid polypeptides, topical form of curcumin, newly formulated artificial tears, diquafosol, rebamipide, tretinoin, and oral uridineseems to be beneficial in the management of ocular lesion associated with sulfur mustard poisoning. Further studies are needed to approve these drugs in SM victims. J. Cell. Biochem. 118: 3549-3560, 2017. © 2017 Wiley Periodicals, Inc.

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Section: Management Of Acute Ocular Lesionsmentioning

confidence: 99%

Ocular Effects of Sulfur Mustard and Therapeutic Approaches

Panahi

Rajaee

Sahebkar

2017

J of Cellular Biochemistry

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“…Previous work has shown that SM vapor applied to the surface of the cornea penetrates to the anterior chamber within minutes, suggesting that the potential exists for endothelial toxicity. 11,19,20 Changes in corneal endothelial morphology of rabbits following SM exposure have been described using specular microscopy, and evidence of endothelial injury has been identified in human MGK corneas, including reduced CEC density with increased variability in size and morphology. 21,22 Although these findings suggest that SM injury may involve an endothelial component, the role of CEC toxicity in the pathophysiology of acute or chronic corneal SM injuries has not been evaluated to date.…”

Section: Involvement Of Endothelial Toxicity In Acute and Chronic Cormentioning

confidence: 99%

Structural, Morphological, and Functional Correlates of Corneal Endothelial Toxicity Following Corneal Exposure to Sulfur Mustard Vapor

McNutt¹,

Tuznik²,

Nelson³

et al. 2013

Invest. Ophthalmol. Vis. Sci.

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Endothelial toxicity occurs at the right time and with the appropriate pathophysiology to contribute to MGK. Based on these findings, we propose a model that explains the relationships among SM dose, the biphasic progression, and the various clinical trajectories of corneal SM injury and that provides a mechanism for temporal variations in MGK onset. Finally, we discuss the implications for the management of SM casualties.

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“…First, early studies reported the development of uveitis in casualties of class III exposures, indicating that SM vapor penetrates through the cornea to react with tissues in the anterior chamber . These findings were corroborated in animal studies demonstrating that radiolabeled SM vapor applied to the corneal surface accumulates in the anterior chamber within minutes . Second, human MGK corneas exhibit histological evidence of reduced endothelial cell density with increased variability in CEC size and morphology .…”

Section: Tissue‐specific Aspects Of Sm Injury: Effects On the Cornealmentioning

confidence: 81%

“…22,23 These findings were corroborated in animal studies demonstrating that radiolabeled SM vapor applied to the corneal surface accumulates in the anterior chamber within minutes. 60,61 Second, human MGK corneas exhibit histological evidence of reduced endothelial cell density with increased variability in CEC size and morphology. 62 These correlations led us to hypothesize that ocular SM exposure can cause acute endothelial toxicity.…”

Section: Tissue-specific Aspects Of Sm Injury: Effects On the Cornealmentioning

confidence: 99%

Contributions of tissue‐specific pathologies to corneal injuries following exposure to SM vapor

McNutt

Tuznik

Glotfelty

et al. 2016

Annals of the New York Academy of Sciences

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Corneal injuries resulting from ocular exposure to sulfur mustard (SM) vapor are the most prevalent chemical warfare injury. Ocular exposures exhibit three distinct, dose-dependent clinical trajectories: complete injury resolution, immediate transition to a chronic injury, or apparent recovery followed by the subsequent development of persistent ocular manifestations. These latter two trajectories include a constellation of corneal symptoms that are collectively known as mustard gas keratopathy (MGK). The etiology of MGK is not understood. Here, we synthesize recent findings from in vivo rabbit SM vapor studies, suggesting that tissue-specific damage during the acute injury can decrement the regenerative capacities of corneal endothelium and limbal stem cells, thereby predisposing the cornea to the chronic or delayed forms of MGK. This hypothesis not only provides a mechanism to explain the acute and MGK injuries but also identifies novel therapeutic modalities to mitigate or eliminate the acute and long-term consequences of ocular exposure to SM vapor.

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The Distribution Kinetics of Topical¹⁴C‐Sulfur Mustard in Rabbit Ocular Tissues and the Effect of Acetylcysteine

Cited by 7 publications

References 20 publications

Ocular Effects of Sulfur Mustard and Therapeutic Approaches

Ocular Effects of Sulfur Mustard and Therapeutic Approaches

Structural, Morphological, and Functional Correlates of Corneal Endothelial Toxicity Following Corneal Exposure to Sulfur Mustard Vapor

Contributions of tissue‐specific pathologies to corneal injuries following exposure to SM vapor

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The Distribution Kinetics of Topical14C‐Sulfur Mustard in Rabbit Ocular Tissues and the Effect of Acetylcysteine

Cited by 7 publications

References 20 publications

Ocular Effects of Sulfur Mustard and Therapeutic Approaches

Ocular Effects of Sulfur Mustard and Therapeutic Approaches

Structural, Morphological, and Functional Correlates of Corneal Endothelial Toxicity Following Corneal Exposure to Sulfur Mustard Vapor

Contributions of tissue‐specific pathologies to corneal injuries following exposure to SM vapor

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The Distribution Kinetics of Topical¹⁴C‐Sulfur Mustard in Rabbit Ocular Tissues and the Effect of Acetylcysteine